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1. Moser AM, Manor E, Narkis G, Kapelushnik J: Imatinib resistant chronic myelogenous leukemia, BCR-ABL positive by chromosome and FISH analyses but negative by PCR, in a child progressing to acute basophilic leukemia: cytogenetic follow-up. Cancer Genet Cytogenet; 2006 Oct 1;170(1):54-7
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  • [Title] Imatinib resistant chronic myelogenous leukemia, BCR-ABL positive by chromosome and FISH analyses but negative by PCR, in a child progressing to acute basophilic leukemia: cytogenetic follow-up.
  • The case of an 11-year-old child with adult-type chronic myeloid leukemia, Philadelphia (BCR-ABL) positive, reverse transcription-polymerase chain reaction negative for the major, minor, and micro breakpoints is presented.
  • In the course of 3 years, the child failed to respond to treatment with hydroxyurea, refused all therapy for 6 months, was intolerant to alpha-interferon and progressed, while on imatinib, to acute basophilic leukemia.
  • A secondary cytogenetic clonal evolution, i(17q), developed during hydroxyurea treatment and a tertiary clonal evolution, +8, was detected during imatinib treatment.
  • It is not clear to what extent the several factors (undefined BCR-ABL breakpoint, treatment avoidance, and initial treatment choices, alone or in combination) played a role in the imatinib relapse and resistance and in the disease progression.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Genes, abl. Leukemia, Basophilic, Acute / surgery. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Bone Marrow Transplantation. Child. Disease Progression. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Reverse Transcriptase Polymerase Chain Reaction


2. Markert E, Siebolts U, Odenthal M, Kreuzer KA, Wickenhauser C: High diagnostic value of morphologic examination and molecular analysis of bone marrow biopsies in a case of BCR-ABL+ CML with clusters of blasts. Int J Hematol; 2009 Apr;89(3):294-7
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  • [Title] High diagnostic value of morphologic examination and molecular analysis of bone marrow biopsies in a case of BCR-ABL+ CML with clusters of blasts.
  • We report a clinical case of chronic myelogenous leukaemia (CML) with regional B-lymphoblastic transformation.
  • Peripheral leukocytosis of 160 x 10(9)/L, splenomegaly and fatigue suggested CML.
  • In peripheral blood and bone marrow smears, white blood cells in all maturation stages and only few blasts were seen and therefore the diagnosis of chronic phase CML was proposed.
  • Cytogenetics performed on peripheral blood cells revealed the characteristic t(9;22)(q34;q11) translocation as solitary abnormality.
  • BCR-ABL FISH analysis demonstrated 31% atypical split signals in the B-lymphoid blasts and in the maturing myeloid cells, furthermore, BCR-ABL fusion transcripts were seen in the RT-PCR assay.
  • Imatinib-based therapy led to temporary regression of peripheral leukocytosis.
  • Bone marrow examination 3 weeks after therapy induction demonstrated considerably reduced cellularity and the proportion of B-lymphoid blasts had decreased to 20% of the nuclear cells.
  • BCR-ABL FISH analysis still presented 21% atypical split signals but levels of BCR-ABL transcripts had significantly fallen indicating a rather favourable prognosis.
  • However, 3 months after diagnosis the patient relapsed and developed an immunodeficiency with soor esophagitis and aspergillus pneumonia.
  • A therapy with dasatinib was not successful and the patient died in consequence of immunodeficiency.
  • This report demonstrates the high diagnostic value of bone marrow biopsy in the evaluation of CML.
  • Besides morphology investigation of diverse methods including RT-PCR and FISH performed on diagnostic bone marrow biopsies are obligatory for ideal monitoring of drug response.
  • [MeSH-major] Bone Marrow / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism

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  • (PMID = 19229589.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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3. Mann G, Trebo MM, Haas OA, Grümayer-Panzer ER, Dworzak MN, Lion T, Gadner H: Philadelphia chromosome-positive mature B-cell (Burkitt cell) leukaemia. Br J Haematol; 2002 Aug;118(2):559-62
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  • [Title] Philadelphia chromosome-positive mature B-cell (Burkitt cell) leukaemia.
  • Philadelphia chromosome-positive (Ph+) acute leukaemia usually shows lymphoblastic morphology and a B-precursor phenotype.
  • The translocation t(9;22) (q34;q11) was seen in 45 out of 50 metaphases, and expression of the corresponding bcr1/abl fusion transcripts, but no IgH/myc co-localization or splitting of c-myc, was demonstrated.
  • Chemotherapy according to the Berlin-Frankfurt-Munster non-Hodgkin's lymphoma (NHL-BFM 95) protocol with maintenance according to the BFM acute lymphoblastic leukaemia (ALL-BFM 90) protocol resulted in continuing complete remission of 54 months.
  • The occurrence of Ph+ Burkitt's leukaemia might reflect multiple-step cancer development.
  • [MeSH-major] Burkitt Lymphoma / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Child. Fusion Proteins, bcr-abl / genetics. Gene Rearrangement, B-Lymphocyte, Light Chain. Humans. Immunophenotyping / methods. Karyotyping / methods. Male. Translocation, Genetic

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  • (PMID = 12139745.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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4. Cilloni D, Saglio G: CML: a model for targeted therapy. Best Pract Res Clin Haematol; 2009 Sep;22(3):285-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CML: a model for targeted therapy.
  • The discovery of the Philadelphia (Ph) chromosome represented the first step towards understanding the molecular basis of haematological malignancies.
  • Subsequent developments including the characterisation of t(9;22)(q34;q11) translocation, the identification of the breakpoint cluster region as well as the demonstration that retrovirally mediated insertion of a human BCR-ABL gene into murine haematopoietic stem cells induced a leukaemia-like picture and the creation of BCR-ABL transgenic mice established the central role of BCR-ABL in chronic myeloid leukaemia (CML) beyond all reasonable doubt.
  • Many years later an important goal was achieved, that is, the use of BCR-ABL as a therapeutic target.
  • However, it is uncertain whether the BCR-ABL fusion gene is really the initiating lesion for the chronic phase of CML.
  • There is an incomplete understanding of the so-called genomic instability that underlies the production of the fusion gene and predisposes the Ph-positive clone to acquire further genetic events leading to advanced-phase disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Delivery Systems / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Animals. Benzamides. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Mice. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 19959080.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 78
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5. Schultheis B, Heissig B, Pasternak G, Hörner S, Hehlmann R: Interferon-alpha-treated patients with chronic myelogenous leukemia show BCR/ABL-positive peripheral blood progenitor cells surviving long-term culture. Folia Biol (Praha); 2000;46(6):251-5
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  • [Title] Interferon-alpha-treated patients with chronic myelogenous leukemia show BCR/ABL-positive peripheral blood progenitor cells surviving long-term culture.
  • Several groups have shown that Ph-progenitors reappear in LTC of CML bone marrow or PBMNC when the cell preparations were derived from newly diagnosed Ph-positive patients or after induction chemotherapy.
  • We have tested the hypothesis whether LTC may further decrease CML progenitors if the cells to be cultured were from IFN-treated patients.
  • In our experiments, PBMNC were cultured from 7 IFN- and 5 HU-treated patients in stable chronic phase of the disease, and from 9 patients at diagnosis.
  • Progenitor cells in PBMNC were quantitatively analyzed before and after 35 days of LTC by combining the clonogenic assay in semisolid medium with dual-color interphase FISH for identification of the BCR/ABL status of colony-forming progenitor cells.
  • A median of 22 colonies (range 7-88) before and 30 colonies (5-71) after LTC were analyzed per patient.
  • Our results show that the number of BCR/ABL-positive CFC before and after LTC was approximately the same.
  • This was independent of IFN or HU therapy.
  • In the IFN group there were 58% (median) BCR/ABL-positive CFC before and 54% (median) after LTC of PBMNC.
  • In the HU group, 80% of CFC were BCR/ABL-positive before and 85% after LTC.
  • A complete elimination of BCR/ABL-positive cells was not achieved.
  • We conclude that CML early progenitors in PBMNC of IFN-treated CML patients may survive LTC.
  • [MeSH-major] Biomarkers, Tumor / blood. Fusion Proteins, bcr-abl / blood. Immunologic Factors / therapeutic use. Interferon-alpha / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplastic Cells, Circulating
  • [MeSH-minor] Antineoplastic Agents, Alkylating / therapeutic use. Humans. Hydroxyurea / therapeutic use. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Chronic-Phase / blood. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / genetics. Leukemia, Myeloid, Chronic-Phase / pathology. Neoplasm, Residual. Tumor Cells, Cultured. Tumor Stem Cell Assay

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  • (PMID = 11140858.001).
  • [ISSN] 0015-5500
  • [Journal-full-title] Folia biologica
  • [ISO-abbreviation] Folia Biol. (Praha)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Biomarkers, Tumor; 0 / Immunologic Factors; 0 / Interferon-alpha; EC 2.7.10.2 / Fusion Proteins, bcr-abl; X6Q56QN5QC / Hydroxyurea
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6. Voskaridou E, Terpos E, Komninaka V, Eftyhiadis E, Mantzourani M, Loukopoulos D: Chronic myeloid leukaemia with marked thrombocytosis in a patient with thalassaemia major: complete haematological remission under the combination of hydroxyurea and anagrelide. Br J Haematol; 2002 Jan;116(1):155-7
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  • [Title] Chronic myeloid leukaemia with marked thrombocytosis in a patient with thalassaemia major: complete haematological remission under the combination of hydroxyurea and anagrelide.
  • The co-existence of thalassaemia major and chronic myeloid leukaemia (CML) is a very rare event.
  • We report a 32-year-old man with thalassaemia major whose progressively increasing leukocytosis and thrombocytosis led to the diagnosis of CML confirmed by the characteristic t(9;22)(q34;q11) chromosomal translocation and the bcr-abl (b3a2) DNA fusion.
  • The administration of hydroxyurea was also associated with a significant HbF increase.
  • [MeSH-major] Antisickling Agents / therapeutic use. Hydroxyurea / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Platelet Aggregation Inhibitors / therapeutic use. Quinazolines / therapeutic use. beta-Thalassemia / complications
  • [MeSH-minor] Adult. Drug Therapy, Combination. Humans. Leukocyte Count. Male. Platelet Count. Remission Induction. Thrombocytosis / blood. Thrombocytosis / complications. Thrombocytosis / drug therapy

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  • (PMID = 11841409.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antisickling Agents; 0 / Platelet Aggregation Inhibitors; 0 / Quinazolines; 0 / anagrelide; X6Q56QN5QC / Hydroxyurea
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7. Thiele J, Kvasnicka HM, Schmitt-Graeff A, Leder LD, Schaefer HE: Changing patterns of histological subgroups during therapy of Ph1+ chronic myelogenous leukaemia. Histopathology; 2000 Oct;37(4):355-62
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  • [Title] Changing patterns of histological subgroups during therapy of Ph1+ chronic myelogenous leukaemia.
  • AIMS: Bone marrow histopathology reveals a striking heterogeneity at diagnosis of Philadelphia chromosome positive (Ph1+) chronic myelogenous leukaemia (CML).
  • However, little information exists on whether these groups represent stable categories of the different classification systems and whether therapeutic regimes exert any influence on the putative shift of histological patterns.
  • There were at least two representative trephines taken at diagnosis and at median intervals of 16 months.
  • These consisted of a granulocytic (51 patients), a predominantly megakaryocytic (73 patients) and a myelofibrotic pattern (49 patients).
  • Follow-up biopsies revealed that a significant transition of histological groups occurred and that, independently of treatment modalities, the myelofibrotic category was associated with an unfavourable prognosis.
  • However, these patients showed no prevalence of either a pre-existing granulocytic or megakaryocytic growth.
  • Myelofibrotic changes were significantly associated with interferon (IFN) and busulfan (BU) therapy.
  • On the other hand, a transition of a myelofibrotic into a nonfibrotic subtype was detectable in 17 of the 49 patients under study and related to hydroxyurea (HU) treatment.
  • CONCLUSIONS: Histological classification systems of bone marrow features in CML do not represent stable patterns, but may be significantly altered by therapy, in particular IFN and HU.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Busulfan / therapeutic use. Granulocytes / drug effects. Granulocytes / pathology. Humans. Hydroxyurea / therapeutic use. Interferon-alpha / therapeutic use. Megakaryocytes / drug effects. Megakaryocytes / pathology. Primary Myelofibrosis / drug therapy. Primary Myelofibrosis / pathology. Recombinant Proteins. Retrospective Studies

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  • (PMID = 11012743.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b; G1LN9045DK / Busulfan; X6Q56QN5QC / Hydroxyurea
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8. Orciuolo E, Buda G, Galimberti S, Cervetti G, Cecconi N, Papineschi F, Petrini M: Complex translocation t(6;9;22)(p21.1;q34;q11) at diagnosis is a therapy resistance index in chronic myeloid leukaemia. Leuk Res; 2008 Jan;32(1):190-1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex translocation t(6;9;22)(p21.1;q34;q11) at diagnosis is a therapy resistance index in chronic myeloid leukaemia.
  • [MeSH-major] Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 6. Chromosomes, Human, Pair 9. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Drug Resistance, Neoplasm. Female. Humans

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  • (PMID = 17418404.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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